Th1 Th2, Tc1 Tc2 cells of patients with otolaryngological diseases

Cytokines are important regulatory mediators secreted by T cells and other immunoactive cells. Based on the cytokine synthesis patterns, CD4 T cells can often be classified into at least two populations with different immune regulatory functions. The Th1 cells, producing interleukin (IL)-2 and inter...

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Bibliographic Details
Main Authors: Nobuo Ohta, Shigeru Fukase, Takeo Fuse, Masaru Aoyagi
Format: Article
Language:English
Published: Elsevier 2004-01-01
Series:Allergology International
Subjects:
Tc1
Tc2
Th2
Online Access:http://www.sciencedirect.com/science/article/pii/S1323893015311175
Description
Summary:Cytokines are important regulatory mediators secreted by T cells and other immunoactive cells. Based on the cytokine synthesis patterns, CD4 T cells can often be classified into at least two populations with different immune regulatory functions. The Th1 cells, producing interleukin (IL)-2 and interferon (IFN)-γ, are often associated with cell-mediated immune responses such as delayed type hypersensitivity (DTH), whereas Th2 cells, secreting IL-4, IL-5 and IL-13, usually provide B cell help and enhance allergic reactions. Naïve CD8 T cells, similar to CD4 T cells, can differentiate into at least two subsets of cytolytic effector cells with distinct cytokine patterns. The Tc1 cells secrete a Th 1 - like cytokine pattern, including IL-2 and IFN-γ. The Tc2 cells produce Th2 cytokines, including IL-4, IL-5 and 11—10. There is increasing evidence that Th1/Th2 and Tc1/Tc2 cytokine imbalance has been of patho- genetic importance in various diseases, such as allergic and autoimmune diseases. The present review article focuses on the evidence that the imbalance of Th1/Th2 and Tc1/Tc2 cytokines plays an important role in various otolaryngological diseases, such as Kimura's disease, Wegener's granulomatosism, acute perceptive hearing loss and Meniere's disease. It is concluded that the predominance of Th 1 or Th2 and Tc1 or Tc2 cells may contribute to the mechanism in the pathogenesis of these otolaryngological diseases.
ISSN:1323-8930